A research team from Juntendo University and the University of Tokyo has discovered a new mechanism that causes internal organs to develop asymmetrically.
The origin of the left-right asymmetry of our internal organs has long been a mystery in developmental biology.The research team has previously discovered that a leftward flow of extraembryonic fluid (nodal flow) occurs in a temporary dent in the body surface of the ventral node, which corresponds to the fetal lower abdomen. have clarified.In addition, as the origin of visceral asymmetry, it was clarified that intracellular calcium increases only on the left side of the ventral node and that left-side-specific signal transduction is induced. The mechanism by which leftward nodal flow produces left-side nodal calcium elevations remains unclear.
In this study, we observed mice in which the PKD1L1 polycystin protein, which is related to intracellular calcium elevation, was made to fluoresce. was found to be shifted to the left.Furthermore, we found that polycystin, which was transported to the left side of the node, binds to nodal protein, which causes an increase in intracellular calcium.Polycystin, which is transported to the left side of the node by nodal flow, is stimulated by nodal proteins to bring about an influx of calcium into the cell, and an increase in intracellular calcium specifically to the left side determines the left-right differentiation of visceral development. It is said that it was suggested as a mechanism.
The results of this research have led to one of the fundamental principles of how the left and right sides of the body develop differently by proposing a new polycystin transfer model, and will greatly contribute to the development of developmental biology.In addition, by elucidating a new extracellular transport mechanism of proteins, various clinical applications are expected, such as the development of anticancer drugs from a new perspective targeting this.
Paper information:[Developmental Cell] Nodal flow transfers polycystin to determine mouse left-right asymmetry